Publication: Defective cytokine production from monocytes/macrophages of E-beta thalassemia patients in response to Pythium insidiosum infection
Issued Date
2019-05-01
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18783279
01712985
01712985
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2-s2.0-85061297311
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Mahidol University
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SCOPUS
Bibliographic Citation
Immunobiology. Vol.224, No.3 (2019), 427-432
Suggested Citation
Somkiat Ud-naen, Tunsuda Tansit, Duangjit Kanistanon, Angkana Chaiprasert, Wanchai Wanachiwanawin, Yuttana Srinoulprasert Defective cytokine production from monocytes/macrophages of E-beta thalassemia patients in response to Pythium insidiosum infection. Immunobiology. Vol.224, No.3 (2019), 427-432. doi:10.1016/j.imbio.2019.02.002 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/51067
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Title
Defective cytokine production from monocytes/macrophages of E-beta thalassemia patients in response to Pythium insidiosum infection
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Abstract
© 2019 Elsevier GmbH Background: Pythium insidiosum has been mainly reported to cause morbidity and mortality in thalassemia patients. P. insidiosum zoospores can germinate to be hyphae within a few hours; therefore, it is difficult to study the initial immune response that P. insidiosum zoospores induce. The present study aims to compare immune responses against P. insidiosum zoospore infection by comparing monocytes/macrophages from thalassemia patients with those from non-thalassemia controls. Methods: In order to keepP. insidiosum in the zoospore stage in vitro for inoculation, the P. insidiosum zoospores were preserved without germination by treatment with inorganic hypochlorite solution. CD14+ cells were isolated from peripheral blood mononuclear cells of thalassemia and non-thalassemia donors and then left to transition to macrophages. Monocytes/macrophage culture was infected with P. insidiosum zoospores and culture supernatants were subjected to Th1/Th2 multiplex cytokine detection. Results: Our study of cytokine production revealed that the basal level of GM-CSF produced by thalassemia monocytes/macrophages was lower than that observed in monocytes/macrophages of non-thalassemia individuals. Higher GM-CSF and IFN-γ response was also found when cells from non-thalassemia people were stimulated with P. insidiosum zoospores compared to thalassemia cells. It was also found that TNF-α, GM-CSF and IFN-γ productions from monocytes/macrophages of thalassemia patients who received iron chelator treatment were significantly higher than those produced from thalassemia patients without iron chelator treatment. Conclusion: For the first time, the present study demonstrates defective immune responses in monocytes/macrophages derived from thalassemia patients in response toP. insidiosum zoospore infection. The results also show an inverse correlation between iron overload and cytokine production in monocytes/macrophages of thalassemia patients. This finding could explain why thalassemia patients are susceptible to P. insidiosum infection.